?/ANTI-? COMPLEXES: STAPHYLOCOCCAL AUREUS PHAGE G1 ORF67

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• 批准号: 8169306
• 负责人: Seth A. Darst
• 金额: $ 0.2万
• 依托单位: CORNELL UNIVERSITY
• 依托单位国家: 美国
• 财政年份: 2010
• 资助国家: 美国
• 起止时间: 2010-04-01 至 2011-03-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/8169306
• 关键词: Bacteria; Bacteriophages; Binding; Biology; C-terminal; Cell physiology; Complex; Computer Retrieval of Information on Scientific Projects Database; Cues; Environment; Funding; Genetic Transcription; Goals; Grant; Growth; Institution; Proteins; Regulation; Regulon; Research; Research Personnel; Resources; Response Elements; Role; Signal Transduction; Source; Staphylococcus aureus; Structure; United States National Institutes of Health; high throughput screening; inhibitor/antagonist; pathogen; response

This subproject is one of many research subprojects utilizing the resources provided by a Center grant funded by NIH/NCRR. The subproject and investigator (PI) may have received primary funding from another NIH source, and thus could be represented in other CRISP entries. The institution listed is for the Center, which is not necessarily the institution for the investigator. Bacterial transcription depends on a primary (group 1) ¿ that is essential for viability. In addition, most bacteria contain alternative ¿'s that control regulons in response to environmental cues. Regulation of ¿ activity is a major mechanism by which bacteria respond to their environment. Many alternative ¿'s are regulated by anti-¿ factors. Despite the structural conservation of ¿'s, anti-¿'s are structurally and functionally diverse, serving as the key response elements to sense and signal environmental cues to the core transcriptional apparatus via the alternative ¿'s. In addition to modulation of ¿ function by cellular anti-¿ factors, many bacteriophages have evolved ingenious mechanisms to inhibit and/or appropriate the host transcription apparatus. The primary ¿ (¿A) of the gram-positive pathogen Staphylococcus aureus (Sau) is targeted by phage proteins that inhibit bacterial growth. Phage G1 ORF67 was identified in a high-throughput screen as a transcriptional inhibitor that binds to the C-terminal domain (domain 4) of Sau ¿A (¿A4). Our goal is to determine the co-crystal structure of G1 ORF67 with Sau ¿A4, and to explore the functional mechanism through which ORF67 inhibits Sau transcription as well as it's role in phage G1 biology.

这个子项目是许多研究子项目中的一个 由NIH/NCRR资助的中心赠款提供的资源。子项目和 研究者（PI）可能从另一个NIH来源获得了主要资金， 因此可以在其他CRISP条目中表示。所列机构为 研究中心，而研究中心不一定是研究者所在的机构。 细菌转录依赖于一个主要的（组1）是生存所必需的。此外，大多数细菌含有替代调节子，可以控制调节子对环境线索的反应。活性调节是细菌对其环境做出反应的主要机制。许多替代品是由反因素调节的。尽管<$s结构保守，反<$s在结构和功能上是多样的，作为关键的反应元件，通过替代<$s感知和信号环境线索的核心转录装置。 除了通过细胞抗噬菌体因子调节噬菌体功能外，许多噬菌体还进化出了巧妙的机制来抑制和/或占用宿主的转录装置。革兰氏阳性病原体金黄色葡萄球菌（Sau）的主要目标是抑制细菌生长的噬菌体蛋白。噬菌体G1 ORF 67在高通量筛选中被鉴定为与Sau <$A（<$A4）的C-末端结构域（结构域4）结合的转录抑制剂。我们的目标是确定G1 ORF 67与Sau <$A4的共晶体结构，并探讨ORF 67抑制Sau转录的功能机制以及它在噬菌体G1生物学中的作用。